Pneumocystis jirovecii detection during mixed pulmonary infection with Guillain-Barré syndrome after multimodal treatment for stage IIIA lung adenocarcinoma: a case report

Background Molecular detection of Pneumocystis jirovecii in an immunocompromised patient does not by itself establish Pneumocystis jirovecii pneumonia (PJP), and respiratory failure may also reflect bacterial infection, postoperative pleural disease, treatment-related lung injury or neuromuscular weakness. Concurrent respiratory infection and Guillain-Barré syndrome (GBS) after multimodal lung-cancer treatment is uncommon and diagnostically challenging. Case presentation A 62-year-old non-smoking woman underwent R0 resection of pT2aN2M0 stage IIIA lung adenocarcinoma followed by pemetrexed-cisplatin chemotherapy and postoperative thoracic radiotherapy. Seven months after surgery, she was admitted with fever and chest tightness and subsequently developed severe oxygen desaturation, impaired consciousness and rapidly progressive limb weakness requiring mechanical ventilation. The calculated admission absolute lymphocyte count was 0.36 × 10⁹/L; Day 7 lymphocyte-subset testing showed a CD4 + T-cell count of 49/µL. Bronchoalveolar lavage fluid tested by targeted multiplex PCR coupled with high-throughput sequencing detected P. jirovecii (476 reads; estimated load < 1.0 × 10³ copies/mL) together with Mycobacteroides abscessus subsp. abscessus, Pseudomonas aeruginosa and viral reads. Because chest CT lacked typical diffuse ground-glass opacities, serum β-D-glucan was < 10 pg/mL and no direct microscopic or immunofluorescence confirmation was available, the patient was treated for mixed pulmonary infection with possible PJP, while colonisation could not be excluded. Cerebrospinal fluid showed protein 0.61 g/L with 4 white cells × 10⁶/L; cerebrospinal-fluid autoimmune encephalitis and ganglioside/sulfatide antibody panels were negative. GBS was suspected clinically, intravenous immunoglobulin was started, and electrophysiology performed after treatment showed a motor-predominant axonal neuropathy. She was extubated, recovered grade 4 limb strength and was discharged for rehabilitation. Conclusions This case illustrates the need to separate pathogen detection from proof of invasive infection and to evaluate pulmonary and neuromuscular causes of respiratory failure in parallel. When weakness accompanies respiratory deterioration after cancer treatment, early neurological examination, cerebrospinal fluid assessment and electrophysiology should complement a structured pulmonary and infectious work-up.